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  • Title: Relation between conduction delay and ventricular fibrillation: characteristics of conduction of premature impulses during acute myocardial ischemia.
    Author: Fujimoto T, Hamamoto H, Peter T, Mandel WJ.
    Journal: Am J Cardiol; 1981 Aug; 48(2):287-94. PubMed ID: 7270438.
    Abstract:
    Critical conduction delay has been shown to be the important factor in reentrant arrhythmias. To determine the causal relation between conduction delay and spontaneous ischemic ventricular fibrillation, conduction delay of induced premature ventricular impulses in the ischemic and the border zones of ventricular myocardium was investigated in 23 dogs. There were 8 control dogs, 9 dogs that manifested ventricular fibrillation within 30 minutes of ligation of the distal left anterior descending coronary artery (group I), and 6 dogs that manifested ventricular fibrillation between 30 and 60 minutes of ligation of the proximal left anterior descending coronary artery (group II). Conduction delay was measured as the change of conduction time from preligation levels to postligation levels in epicardial and endocardial sites in both base to apex (anterograde) and apex to base (retrograde) directions. Conduction delay in all four directions was compared in the control group and groups I and II (ventricular fibrillation). By means of continuous recordings on tape, the origin of ventricular fibrillation was determined to be in the ischemic zone (13 of 15 dogs) or in the border zone (2 of 15 dogs). Conduction delay in all directions was greater in the group with ventricular fibrillation whether the fibrillation occurred after the first or second ligation. Specifically, epicardial anterograde conduction (in the border zone) and retrograde conduction (in the ischemic zone) were significantly delayed in group I. Conduction in group II was significantly delayed in both the ischemic and the border zones in three of four directions at 35 minutes. The rate of change of conduction time in all four directions was significantly greater in the group with ventricular fibrillation than in the control group. Pending further work, this model may provide a reliable marker for the development of spontaneous ventricular fibrillation during acute myocardial ischemia and may permit assessment of various interventions as specific therapy for acute reentrant ischemic tachyarrhythmias leading to ventricular fibrillation.
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